Recent advances in the field of DNA repair are providing a solid mechanistic basis for understanding the biological consequences of damaged cellular DNA. It is becoming increasingly clear that faulty processing of damage in unique regions of the genome can result in aberrant growth control leading to malignancy. Thus, protooncogenes can be activated by mutation at specific nucleotide sites, by amplification, or by transposition to certain genomic locations. Additionally, some cancer-prone hereditary diseases have been shown to involve defects in the processing of damaged DNA. Many genes involved in DNA repair now have been cloned and their protein products identified, and multienzyme repair complexes analogous to those utilized in DNA replication are being characterized. Factors controlling the fidelity of replication and the consequences of attempted replication at sites of lesions are being elucidated, and the role of chromatin structure and gene expression in the accessibility of damage to repair is becoming understood. Finally, powerful new probes including specially constructed shuttle-vectors are being utilized to understand DNA damage processing in mammalian cells in which genetic analysis has lagged behind that in simpler systems. This meeting will provide an opportunity for workers in diverse areas of the DNA repair field to gain increased awareness of promising new systems and approaches. The field of DNA repair is rapidly approaching the level of sophisticated biochemical understanding that has been achieved with replication and recombination. This conference will document and develop the most significant advances in this field in the five year period since the last UCLA Symposium on this topic.